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鼻窦炎中的神经源性机制。

Neurogenic mechanisms in rhinosinusitis.

作者信息

Baraniuk J N

机构信息

Division of Rheumatology, Immunology and Allergy, Georgetown University Medical Center, GL-020 Gorman Building, 3800 Reservoir Road, Washington, DC 20007-2197, USA.

出版信息

Curr Allergy Asthma Rep. 2001 May;1(3):252-61. doi: 10.1007/s11882-001-0016-4.

Abstract

Nasal sensory nerve stimulation leads to sensations of pain and congestion and nociceptive nerve axon response-mediated release of substance P that stimulates glandular secretion as an immediate-acting protective mucosal defense. Recruited parasympathetic reflexes cause submucosal gland secretion via muscarinic M3 receptors. Parasympathetic reflexes, sneezing, and other avoidance behaviors rapidly clear the upper airway of offending agents while protecting the lower airways. Dysfunction contributes to allergic, infectious, and other nonallergic rhinitides and possibly sinusitis. Sympathetic arterial vasoconstriction reduces mucosal blood flow, sinusoidal filling, and mucosal thickness, restoring nasal patency. Loss of sympathetic tone may contribute to some chronic, nonallergic rhinopathies.

摘要

鼻感觉神经刺激会引发疼痛和充血感,伤害性神经轴突反应介导的P物质释放会刺激腺体分泌,这是一种即时起作用的保护性黏膜防御机制。募集的副交感神经反射通过毒蕈碱M3受体引起黏膜下腺分泌。副交感神经反射、打喷嚏及其他回避行为能迅速清除上呼吸道中的致病因子,同时保护下呼吸道。功能障碍会导致过敏性、感染性及其他非过敏性鼻炎,还可能引发鼻窦炎。交感神经动脉血管收缩会减少黏膜血流量、窦状隙充盈和黏膜厚度,恢复鼻腔通畅。交感神经张力丧失可能导致一些慢性非过敏性鼻病。

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